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By Dr. Salah A. Ismail Assistant Professor of Anesthesia Faculty of Medicine, King Faisal University 2007/2008

Describe the management of temperature changes. Describe the management of neurological complications of general anesthesia. . Describe the management of postoperative nausea and vomiting. Describe the management of cardiovascular complications of general anesthesia.OBJECTIVES At the end of this lecture. Describe the management of adverse drug reactions and hypersensitivity. Describe the management of respiratory complications of general anesthesia. the student should be able to: • • • • • • • • Enumerate the complications of general anesthesia. Describe the management of complications of position.

Hypoventilation VI.Aspiration pneumonia  Cardiovascular complications I.Respiratory obstruction III.Perioperative neuropathy  PONV  Temperature changes: Hypothermia and hyperthermia  Adverse drug effect and hypersensitivity  Complications of positioning  Miscellaneous .Awareness II.Arrhythmias  Neurological complications I.Complications of laryngoscopy and intubation II.Delayed recovery III.Hypoxemia IV.Hypercapnia and hypocapnia V.Hypotension II.Hypertension III.Complications of general anesthesia  Respiratory complications I.

Cuff perforation . ETT obstruction c. Laryngospasm c.Complications of laryngoscopy and intubation 1. b. f. Dislocated mandible. 3.A) Respiratory complications I. Edema of glottis or trachea. Pressure injury on trachea. e. Sympathetic stimulation b. Errors of ETT positioning: a. Position of the cuff in the larynx 2. d. Endobronchial intubation c. Airway trauma: a. Post intubation granuloma of vocal cords. ETT malfunction: a. c. Physiologic responses to airway instrumentation: a. Bronchospasm 4. Risk of ignition b. Esophageal intubation b. Sore throat. Tooth damage.

and vocal cord paralysis. e. At the lips. By the tongue c. 7. Noisy breathing (unless obstruction is absolute and complete). Retraction of the chest wall and of the supraclavicular. relaxed vocal cords and FB. 5. 6. At the glottis: laryngeal spasm. Causes: include incomplete anesthetic recovery. Faults of apparatus: Kink or obstruction of ETT  Upper airway obstruction in PACU A. The natural heave of the chest and abdomen becomes replaced by an indrawing of the upper chest and an outpushing of the abdomen because of strong diaphragmatic action. Cyanosis. infraclavicular and suprasternal spaces. Airway . Inadequate tidal volume. airway edema. Above the glottis d. 3.II. 4. Bronchospasm f. Sites of obstruction: a. laryngospasm. 2. b. wound hematoma. Excessive abdominal movement.Respiratory obstruction: Signs: 1. Use of accessory muscles of respiration.

III. inhalation of racemic epinephrine.Treatment of laryngospasm: initial treatment includes 100% oxygen. tachycardia. Reintubation with a smaller tube may be helpful. cardiac arrhythmias. B. and gentle CPAP (may be applied by face mask). If laryngospasm persists and hypoxia develops. Decreased FiO2 2. and hypotension) are nonspecific. Laryngospasm and laryngeal edema A. B.Treatment of glottic edema and subglottic edema: administer humidified oxygen by mask. V/Q mismatch 4. Increased O2 utilization by tissues 5. Hypoventilation 3. head-tilt. succinylcholine (0. hydrocortisone IV may be considered. bradycardia. Tissue hypoxia Clinical signs of hypoxia (sweating.obstruction in unconscious patients is most commonly due to the tongue falling back against the posterior pharynx.Hypoxemia: PaO2 less 60 mmHg or SaO2 less 90% Causes: 1. Treatment: supplemental oxygen while corrective measures are undertaken. oral or nasal airways. repeated every 20 minutes. hypotension. C. Triggering stimuli include pharyngeal secretions extubating in stage 2. Definition: Laryngospasm is a forceful involuntary spasm of the laryngeal musculature caused by sensory stimulation of the superior laryngeal nerve.0 mg/kg. . and cardiac arrest are late signs. anterior mandibular displacement. The large negative intrathoracic pressures generated by the struggling patient in laryngospasm can cause pulmonary edema. 10-20 mg).25-1. hypertension. Jaw thrust.

Causes: 1. Decreased chest wall compliance e. Increased intrapulmonary shunting relative to closing capacity is the most common cause of hypoxemia following general anesthesia. Pain c. CV stroke 3.Peripheral factors a. B. Marked hypoventilation may require controlled ventilation until contributory factors are identified and corrected. .Respiratory obstruction 2. Pneumo or hemothorax. C. Muscle weakness b. Causes: 1. treatment of the cause.Hypoventilation 3. d. Respiratory depressant drugs b. Hypothermia c. e.Increased FiCO2 2.Increased CO2 production by tissues Treatment: of the cause. Hypoventilation in the PACU is most commonly caused by residual depressant effects of anesthetic agents on respiratory drive or persistent neuromuscular blockade. Treatment: should be directed at the underlying cause. Additionally.Factors affecting the ventilatory drive a. kyphoscoliosis. V) Hypoventilation A. Treatment: oxygen therapy with or without positive airway pressure. IV) Hypercapnia PaCO2 or ETCO2 > 40 mmHg.g. Decreased diaphragmatic movement.Increased dead space 4.

In the surgical patient it is most likely to occur at induction or during emergence from anaesthesia. particularly if .Aspiration of material with a pH less than 2. such decreased consciousness and impaired cough or gag reflexes. However. Pathophysiology  The clinical consequences of pulmonary aspiration are variable.VI. Bronchospasm often occurs and auscultation of the chest may reveal wheeze and crepitations. Aspiration at induction or emergence from anesthesia may be obvious with gastric contents at the oropharynx and in the trachea at laryngoscopy. Manifestations: They vary depending on the degree of aspiration.Pulmonary aspiration Aspiration is defined as the inhalation of material into the airway below the level of the true vocal cords. saliva. tachycardic and tachypnoeic.5 causes extensive lung damage. mediated in particular by the activation of neutrophils. leading to pulmonary edema. Fluid and protein leak into the alveoli and bronchi. An inflammatory cascade is triggered in the lungs. The result is ventilation–perfusion mismatch and consequent hypoxia.  In severe cases of aspiration the resulting acute lung injury is global. . Incidence and severity increase in emergency cases. especially patients with delayed gastric emptying such as CS. intestinal obstruction. it may occur silently. result in pulmonary atelectasis. aspirated material settles in the posterior segment of upper lobes and superior segment of lower lobes particularly in the right lung. The patient may become hypoxic. The material may include foreign bodies. In supine patients. and surfactant dysfunction. However.  The primary determinants are the nature of the material aspirated and the host’s response to it.Aspiration of solid particles may result in upper airway obstruction or localized atelectasis. Alveolar epithelial and endothelial damage. Pulmonary aspiration occurs as the protective airway reflexes are lost. damage may be localized. . nasopharyngeal secretions or gastric contents.

the oropharynx suctioned and the patient placed in a left lateral head-down position. In severe cases. Lung protective strategies should be used to limit further lung injury caused by mechanical ventilation. oxygenation may be improved by using positive end-expiratory pressures of up to 10 airway device other than a cuffed orotracheal tube is used during anesthesia. Most patients will be extubated and managed with supplementary oxygen. intubation should proceed immediately. Airway pressures increase in patients receiving volume-controlled ventilation and tidal volumes decrease in those who are ventilated using pressure-controlled ventilation. Using low tidal volumes of 4-6 ml/kg with increased ventilation frequency to maintain minute volume reduces pulmonary injury. Once the airway is secure. suction any remaining gastric contents via a large bore nasogastric tube.If the patient is apneic. . Cricoid pressure should not be applied if the patient is vomiting because the high intra-oesophageal pressures generated may result in rupture. if the patient remains hypoxic with oxygen saturations below 90% on 100% oxygen then they should remain intubated and be transferred to the ICU. blood gas monitoring and sputum culture. . The airway should be suctioned via the tracheal tube before positivepressure ventilation begins. However. Investigations include chest radiographs. Surgery should be abandoned or postponed if possible. the oropharynx must be suctioned and the patient placed in the recovery position. . Management The risks of aspiration in patients undergoing general anaesthesia should be reduced. . Initial management: .If the patient is conscious and breathing. then cricoid pressure should be applied.If the patient is unconscious and breathing. in general. Patients at high risk must be identified. However. Further management: intensive care management of patients with aspiration pneumonia is supportive. ventilation should not be delayed.Administer 100% oxygen and reduce the risk of further aspirate contaminating the airway. if the patient is severely hypoxic. to avoid contaminating the distal airways further.

hypervolemia. such that antibiotic therapy is not required. III. nitroprusside or nitroglycerin.Treatment: fluid challenge. epinephrine) and alpha receptor agonists (phenylephrine). Long-term sequelae of pulmonary aspiration include the development of lung abscesses and empyema.Bronchodilators such as salbutamol and ipratropium bromide can be given to relieve bronchospasm. various medications can be used to treat hypertension including beta blockers. which are best identified using chest CT. hypovolemia. Hypertension A. Cardiac dysrhythmias . cardiac tamponade. The use of steroids has not been shown to improve survival.Causes: hypoxemia. and vasopressors. preoperative hypertension.Treatment: correction of the initiating cause. calcium channel blockers. pulmonary embolus. decreased myocardial contractility (myocardial ischemia. Specific therapy includes the use of fibreoptic bronchoscopy to identify and remove particulate matter. CVP and PA catheter monitoring may be needed to guide therapy. Causes: enhanced SNS activity (pain. B. B. hypoxemia. bladder distension). pulmonary edema). decreased systemic vascular resistance. Bronchial culture must be used to guide the use of antibiotic therapy. Hypotension A. Acid aspiration is usually sterile and causes a pneumonitis rather than an infective pneumonia. increased intracranial pressure. pneumothorax. cardiac dysrhythmias. pharmacologic treatment includes inotropic agents (dopamine. II. dobutamine. B) Hemodynamic Complications I.

persist for months or years.2% Increased in obstetric. b. . . Intraoperative: . cardiac anesthesia and hypovolemic patients.g. electrolyte and acid-base imbalance. . hypothermia. anxiety and fear of death.Postoperative psychic trauma e.Machine malfunction c. sleep disturbances.C/P: Postoperative psychic trauma e. Causes: a-Limited doses of anesthetic agents.g.Awareness: Incidence: 0. sensation of paralysis and pain). but accompanied by conscious recall of events (unpleasant sensations e. pain. insomnia. Preoperative: . Implicit memory: . auditory and visual perception.Preoperative check of equipments and anesthetic machine . but not accompanied by conscious recall of events. increased ICP.Informed consent B. B.C/P: Intraoperative stress that causes sympathetic stimulation. dreams. depression.Preoperative visit . hypercarbia. digitalis toxicity. hypovolemia. sleep disturbances. depression. Explicit memory: . Types of patient awareness during anesthesia: 1. Causes: hypoxemia.Increased dependence on muscle relaxants Measures for prevention: A.The information is retained in the memory.The information is retained in the memory. insomnia. C) Neurologic Complications I.g. 2. anxiety and fear of death. .A.continuous monitoring of depth of anesthesia .Treatment: of the cause. anticholinesterases and malignant hyperthermia. dreams. myocardial ischemia.

2.. hypertension. hyperglycemia. old age. atherosclerosis. 3. Stretch (traction) 2. II. renal and liver diseases.visit the patient. minimum MAC 0. avoid muscle relaxants unless indicated. hypercapnia. hypothyroidism.Delayed recovery: Causes: (1) Metabolic and electrolyte causes: Hypoglycemia. III. C. hypoalbuminemia. Direct surgical trauma Risk Factors: 1. previous CNS lesions and cardiovascular and cranial surgery caused by severe hypotension or hypertension. Prolonged surgery. Compression 4.8. hyponatremia. (3) Cerebral depression by drugs: Risk factors: Hypothermia. Postoperative: . cimetidine and B-blockers. hypocapnia. renal and hepatic failure. . (2) Cerebral hypoperfusion: Risk factors are old age.Psychotherapy. Old age. Management: detect and treat the cause. ch. hypoxia. High body mass index ≥38. supplement opioid-based anesthesia with potent inhalational or IV agents. cerebral embolism and Hge. hypokalemia. . Metabolic causes 5.Apology .Perioperative Neuropathy: Causes 1.Anesthetic techniques: Amnestic agents.

and slight hip flexion. forearm supination. 5. Pad lateral aspect of upper fibula. sitting Any Avoid stretching or direct compression at neck or axilla. Padding at elbow. padding. reverse Trendelenburg Any Especially lithotomy Prevention Maintain venous pressure above 0 at the wound. 8. lateral decubitus Any Any Prone. Avoid compression of lateral humerus. Complications of positioning Complication Air embolism Backache Compartment syndrome Position Sitting. Some anatomic variations. Lumbar support.4. Hypotension. Prolonged postoperative bed rest. Padding over bony prominences. 6. DM. Avoid pressure on globe. D) Postoperative Nausea and Vomiting . Vascular disease. Taping and/or lubricating eye. Preexisting chronic nerve dysfunction. Corneal abrasion Especially prone Nerve palsies Brachial plexus Any Common peroneal Radial Ulnar Retinal ischemia Skin necrosis Lithotomy. Maintain perfusion pressure and avoid external compression. 7. 9. prone.

C. ophthalmic. ketamine). including. causing the release of chemical mediators. leukotrienes. young age. regional anesthesia. B. D. . gastroparesis. histamine.Risk factors A. and plastic surgery. anticholinesterase reversal agents. gastric distention. Anesthesia-related factors: premedicants (morphine and other opioids). E) Allergic Drug Reactions 1. tachycardia. Postoperative factors: pain. prostaglandins. anxiety. Ondansetron. duration of surgery. Anaphylaxis A. Surgery-related factors: gynecological. longer duration of anesthesia. obesity. etomidate. Dexamethasone. Promethazine. Patient risk factors: short fasting status. This reaction is initiated by antigen binding to immunoglobulin E (IgE) antibodies on the surface of mast cells and basophils. inhalational agents. kinins. Cardiovascular: hypotension. Anaphylaxis is an allergic reaction which is mediated by an antigen-antibody reaction (type I hypersensitivity reaction). Metoclopramide. methohexital. endocrine effects of surgery. abdominal. B. Combination therapy is the most effective. Dolasetron. female. mask ventilation. Clinical manifestations of anaphylaxis 11. ENT. history of postoperative nausea/vomiting or motion sickness. movement after surgery. dizziness. opioid administration. Granisetron Propofol 10-20 mg IV. pain. premature oral intake. intraoperative pain medications. and platelet-activating factor. dysrhythmias. anesthetics agents (nitrous oxide. Treatment of Postoperative Nausea and Vomiting (PONV) Droperidol.

Secondary treatment 11. Dermatologic: urticaria.5 mg IV for cardiovascular collapse). .1-0. Epinephrine (10-100 mcg IV bolus for hypotension.22. 54. 2. 66. laryngeal edema. Airway evaluation (prior to extubation). Discontinue drug administration and all anesthetic agents. Aminophylline 5-6 mg/kg IV over 20 minutes. 7 Temperature changes I) Hypothermia: It is unintentional decrease of core body temperature to < 35 C during anesthesia Causes: 1. Although the mechanisms differ. B.25-1 gm hydrocortisone.Central inhibition of thermoregulation. 55.Drop in core temperature. 3. anaphylactic and anaphylactoid reactions can be clinically indistinguishable and equally lifethreatening. norepinephrine 2-4 mcg/min.5-1 mEq/kg. 33. Antihistaminic medications IV. Epinephrine 2-4 mcg/min. 22. 1-2 grams methylprednisolone or 0. cough. Initial therapy 21. 33. 0. 43. Anaphylactoid reactions resemble anaphylaxis but are not mediated by IgE and do not require prior sensitization to an antigen. Anaphylactoid reactions 1A. 32. Intravenous fluids (1-5 liters of LR). pruritus. Treatment of anaphylactic and anaphylactoid reactions 1A. B. hypoxemia. Sodium bicarbonate 0. Pulmonary: bronchospasm. Administer 100% oxygen. facial edema. pulmonary edema. dyspnea. 44. 2.

Pethidine 25 mg. inhalational anesthetics. enflurane.More common after hypothermia.warm mattress and blanket 6.increased myocardial ischemia. and succinylcholine.Heat loss by radiation. desflurane. isoflurane. prolonged surgery. evaporation. Shivering . Effects: . .Extremes of age.use low flow anesthesia. anticholinergic premedication. the body cannot compensate for hypothermia.humidify the inspired gases 5. Mechanism: May be due to alteration in the descending control of spinal reflexes after GA.warm solutions 3. II) Malignant Hyperthermia 1. Definition: It is a fulminant skeletal muscle hypermetabolic syndrome occurring in genetically susceptible patients after exposure to an anesthetic triggering agent.increased CO2 production .increase ambient temp and humidity 2. Contributing factors: .increased O2 consumption . . female in the luteal phase. Prevention: 1. sevoflurane.enclose exposed viscera 4.By interfering with the hypothalamic function (decreased VC and shivering threshold and increased sweating threshold) so. convection and conduction.O2 .increased CO and minute ventilation .normothermia . Treatment: . cold infusion or irrigation fluids. Triggering anesthetics include halothane. muscle relaxants.

skeletal muscle swelling. up to 70% without dantrolene therapy. arrhythmias. E. renal failure. left heart failure. B. Early therapy reduces mortality for less than 5%. Adults: approx 1:40. Mortality: 10% overall. approx 1:220. Muscle rigidity and masseter spasm in the presence of neuromuscular blockade. 4. mottling. Late (6-24 hours) signs: pyrexia. B. sweating.2. unstable blood pressure. C. and myoglobinuria. resulting in a sustained muscle contraction.000 general anesthetics when agents other than succinylcholine are used. rapid temperature increase.000 general anesthetics when succinylcholine is used. hypoxemia. hepatic failure. calcium. tachypnea. The presence of a large difference between mixed venous and arterial carbon dioxide tensions confirms the diagnosis of malignant hyperthermia. Early signs: tachycardia. 3. Etiology: the gene for malignant hyperthermia is the genetic coding site for the calcium release channel of skeletal muscle sarcoplasmic reticulum. Children: approx 1:15. Incidence and mortality A. C. Familial autosomal dominant transmission. myoglobin. tachypnea. DIC. D. The syndrome is caused by a reduction in the reuptake of calcium by the sarcoplasmic reticulum necessary for termination of muscle contraction. F. Anesthesia for malignant hyperthermia susceptible patients . 5. CPK. D. Laboratory: respiratory and metabolic acidosis. increased serum levels of potassium. hypercarbia (increased end-tidal CO2 is the most sensitive clinical sign). Signs of onset: tachycardia. and cola-colored urine. Clinical findings A. cyanosis.000 general anesthetics.

Ca. B. use new circuit and soda lime. 10-20 u. Pretreatment with dantrolene is not recommended. Hyperkalemia: correct with bicarbonate or with glucose. Hyperventilate: 100% oxygen. Labs: PT. Malignant hyperthermia treatment protocol A. PTT. 3. C. F. platelets.5 mg/kg IV over 10-30 minutes prior to induction. rectum. C. G. mannitol 0. E. repeat every 5-10 minutes until symptoms are controlled or a total dose of up to 10 mg/kg is given. conclude surgery as soon as possible. lactate. CPK. Maintain urine output >1-2 mL/kg/hr. Lavage stomach. and regular insulin. H. Administer dantrolene 2. D. Actively cool patient 1. 6. If deemed necessary. high flows. Correct metabolic acidosis: administer sodium bicarbonate. Follow with ABG. Malignant hyperthermia may be triggered in susceptible patients who have had previous uneventful responses to triggering agents. 25-50 gm IV. K.A. bladder.5 mg/kg IV. peritoneal and thoracic cavities. Surface cooling with ice and hypothermia blanket. Fresh carbon dioxide absorbent and fresh delivery tubing are also recommended. . ABG. may give 2. urine myoglobin. 1-2 mEq/kg IV guided by arterial pH and paCO2.25 g/kg IV or furosemide 1 mg/kg IV (up to 4 times) and/or hydration. I. Consider invasive monitoring: arterial blood pressure and CVP. B. Iced IV NS (not LR) 15 mL/kg every 10 minutes times three if needed. Continue with safe agents if surgery cannot be stopped. Stop triggering anesthetic agent immediately. If needed. Changing the fresh gas hose will hasten the reduction of the concentration of inhalation agents. 2. The anesthesia machine should be prepared by flushing the circuit with ten liters per minute of oxygen for 20 minutes.

 Calcium channel blockers should not be given when dantrolene is administered because hyperkalemia and myocardial depression may occur.J. Postoperatively: continue dantrolene 1 mg/kg IV q6 hours x 72 hrs to prevent recurrence. .5 mL/kg/hour) most likely reflects decreased renal blood flow due to hypovolemia or decreased cardiac output. G) MISCELLANEOUS Renal dysfunction: Oliguria (urine output less then 0. Observe in ICU until stable for 24-48 hrs.